Taurine (2-aminoethanesulfonic acid) is a sulfur-containing free β-amino acid. As an aminosulfonic acid, taurine cannot form peptides. Taurine is considered semi-essential in mammals.
A healthy person has 50 to 70 g of taurine in their body.
Taurine has therapeutic significance for
-
ADHD
- neurological developmental disorders
- Angelman syndrome
- Fragile X syndrome
- Sleep-wake disorders
- Neural tube defects
1. Taurine synthesis¶
Taurine biosynthesis mainly takes place peripherally in the liver via the methionine - cysteine - cysteine sulphonic acid - hypotaurine - taurine pathway.
In the brain, taurine is synthesized in the hippocampus and cerebellum by conversion of the amino acid cysteine by sulfinic acid decarboxylase (taurine synthase and CAD/CSAD).
Taurine can cross the blood-brain barrier. However, unlike all other neuroactive amino acids, taurine consists of sulfonic acid rather than carboxylic acid, which makes it more difficult to cross the blood-brain barrier
In humans, the rate of taurine biosynthesis in the liver is low, making the diet the most important source of taurine.
Taurine is contained in colostrum (first milk, colostrum, colostrum) as well as usually in infant formula and parenteral solutions.
Cooking does not affect the taurine content. Taurine is found in food
- in large quantities in
- Shellfish, especially mussels, scallops and clams
- dark meat from chickens and turkeys
- some energy drinks (e.g. 1000 mg / 250 ml)
- in small quantities in
2. Effects of taurine¶
Taurine can be found in
- Brain
- Retina
- Heart
- Placenta
- Leukocytes
- Muscles
Taurine influences signal transmission in the brain. It stimulates the influx and membrane binding of calcium and supports the movement of sodium and potassium through the cell membrane. This increases contraction and has an anti-arrhythmic effect on the heart. As an antioxidant, taurine protects tissue from oxidative damage.
In the developing brain, the taurine concentration in the first postnatal week is 3-4 times higher than in the adult brain.
Taurine works
- soothing in relation to
- Consequences of inflammation and oxidative stress
- neurodegenerative diseases
- Stroke
- Epilepsy
- diabetic neuropathy
- protective in relation to
- Injuries / poisoning of the nervous system
- oxidative stress
- Parkinson’s disease
- Alzheimer’s disease
- Huntington
- modulating / regulating
- Brain development
- Development of the optical system (retina)
- Immune system
- Stress of the endoplasmic reticulum
-
Protein quality control; taurine (like other organic osmolytes) promotes proper protein folding and membrane trafficking of the mutant CFTR protein (delta508 CFTR), which does not pass from the ER to the plasma membrane without organic osmolytes
-
Ca2+ homeostasis
-
neuronal activity and excitability at the molecular level
- Learning and memory
- Aggression inhibition
- Energy metabolism
- Gene expression
- Osmosis
- Reproduction
- Stabilization of membranes
- Regulation of the heart muscle
- suppresses the formation of reactive oxygen species
- inhibits cellular apoptosis
Whether taurine boosts the metabolism by influencing insulin levels is an open question.
Taurine has a blood pressure-lowering effect.
Taurine and salt can lead to an excessive sodium content in the cells, which can be life-threatening.
According to a statement by the European Food Safety Authority, the NOAEL (No Observed Adverse Effect Level) for taurine is 1000 mg/kg per day.
Taurine influences
- Synapsin 1
- crucial for the development of synapses
-
Postsynaptic density protein-95 level
- crucial for the development of synapses
- Proliferation of stem/progenitor cells
- increased survival rate of newborn neurons, improved neurogenesis in adulthood
- antidepressant effect and protective effect against mild unpredictable stress, possibly due to
- Regulation of the HPA stress axis
- Promotion of the formation, survival and growth of neurons in the hippocampus
Offspring of mothers with taurine deficiency show a lower brain weight and abnormal morphologies in the visual cortex and in the cerebellum
Taurine deficiency often correlates with kidney failure and immune system disorders, especially increased inflammation.
Mice without a functioning taurine transporter (TauT-KO mouse):
- Loss of long-term potentiation in the striatum
- impaired GABAergic inhibition in the striatum, which can influence anxiety behavior
- less anxiety-like behavior in the elevated plus maze test
- Hearing problems
- a lower body weight
- Motion intolerance
- skeletal muscle atrophy
- various diseases at an advanced age
- mild cardiomyopathy (unclear)
- for this
- on the other hand
- Blindness
- Odor disorders
- non-specific hepatitis
-
chronic liver fibrosis
- shortened life expectancy
- 591 days in TauT-KO mice
- 795 days for non-TauT-KO littermates
A one-week course of taurine significantly reduced the levels of 17 cytokines and increased the level of one:
-
IL-1α, IL-1β, IL-4, IL-5, IL-6, IL-10, IL-12p70, IL-13, IL-17, tumor necrosis factor (TNF)-α, interferon-gamma, eotaxin, granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, leptin, monocyte chemotactic protein-1 and vascular endothelial growth factor (VEGF) decreased
- Macrophage inflammatory protein 1 alpha increased
Taurine effectively reversed the severity of traumatic brain injury by
- Cerebral edema decreased
- the increased activity of the astrocytes reduced
- reduced the proinflammatory cytokines
Taurine tonically activates GABA-A receptors in the thalamus.
Taurine stimulated ERK I/II activity in the presence of AMPA or H2O2. This could be relevant for dopamine uptake by DAT and thus for ADHD.
Taurine appears to regulate neurotransmitter actions and the synaptic receptivity of entire brain regions. Taurine could influence the extent to which the respective brain region is capable of neuronal information processing and can regulate behavior. The taurine level in a brain region could serve as an index for the regional reactivity to synaptic input signals and thus for the function of the brain region in question as a whole. Consequences, the observed changes in taurine levels in adult rats that received MPH during adolescence could
can explain the hyperfunction of the dorsal striatum and the correlating hypofunction of the nucleus accumbens.
3. Taurine for ADHD¶
We could not find any studies on the effect of orally ingested taurine on extracellular or phasic dopamine.
Taurine injected into the abdominal cavity reduced extracellular dopamine levels in the striatum. Intrastriatal infused taurine increased the extracellular dopamine concentration in the striatum, while it was decreased intranigrally.
In ADHD, extracellular dopamine is reduced and phasic dopamine is increased. See under ADHD - Disorders of the dopamine system In the Dopamine section in the Neurological aspects chapter. An increase in extracellular dopamine, e.g. through reduced dopamine reuptake or increased DAT efflux, would therefore be helpful.
Taurine has so far only been mentioned in a few reports as a possible ADHD medication.
A study on rats came to the conclusion that taurine can have positive effects on ADHD.
- Low dew rates increased
- The DAT in the striatum significantly (only) in WKY rats (a non-ADHD animal model)
-
Dopamine uptake in the striatum in both SHR and WKY rats.
- High-dose taurine reduces (only) in SHR rats (which represent an animal model of ADHD-C with hyperactivity)
- The DAT in the striatum significantly
-
DAT in the striatum are increased in ADHD
-
Dopamine uptake in the striatum
-
Dopamine (re)uptake in the striatum is increased in ADHD
- Interleukin (IL)-1β and C-reactive protein
- The horizontal movement
- The functional connectivity of the hippocampus (also in WKY)
- The mean amplitude of low-frequency fluctuations (0.01-0.08 Hz) (mALFF, mean amplitude of low-frequency fluctuation (mean ALFF)) in the hippocampus on both sides (also in WKY)
- Both low and high dew amounts increase
- Significantly increased BDNF levels in the striatum of both SHR and WKY rats
BDNF is reduced in ADHD
High-dose taurine reduced hyperactivity in SHR rats by decreasing inflammatory cytokines and modulating functional brain signaling:
- WKY with high dew yield
-
CRP (C-reactive protein) significantly reduced in serum
-
SHR with low or high dew content
- Interleukin (IL)-1β significantly reduced
-
CRP significantly reduced
- WKY and SHR with low dew point
- horizontal locomotion significantly increased
-
SHR with high dew point
- horizontal locomotion significantly reduced compared to SHR control group
- WKY like SHR with high dew point
- functional connectivity (FC) significantly reduced
- mean amplitude of the low-frequency fluctuation (mALFF) in the bilateral hippocampus significantly reduced
-
SHR with low or high dew content
- mALFF significantly reduced compared to SHR control group
In people with ADHD, a small study found that
- A reduced ALFF
- In the right inferior frontal cortex
- In the cerebellum on both sides
- In the missing
- An increased ALFF
- In the right anterior cingulate cortex
- In the left sensorimotor cortex
- In the brain stem on both sides
In contrast, a very comprehensive study with 985 test subjects found significant differences, but also not in the hippocampus. Another small study found no correlation between ALFF and ADHD.
A high consumption of energy drinks with taurine could represent self-medication. One serious disadvantage is the immense amount of sugar and caffeine in these drinks. At the same time, a significant number of people with ADHD report a very high consumption of sugar and caffeine from the time before their medication was discontinued.
4. Taurine for Parkinson’s disease¶
Taurine protected dopaminergic cells by inactivating microglia-mediated neuroinflammation:
Taurine suppressed microglial activation induced by paraquat or maneb. When microglia were reduced, this abolished the dopaminergic neuroprotective effects of taurine.
Taurine suppressed paraquat- or maneb-induced microglial M1 polarization and gene expression of proinflammatory factors.
Taurine inhibited the activation of NADPH oxidase (NOX2) by interfering with the translocation of the cytosolic subunit p47phox and the nuclear factor kappa B (NF-κB) signaling pathway, both of which are key factors in the initiation and maintenance of the microglial M1 inflammatory response.